The menstrual cycle in woman is composed of three distinct phases (Yen S, and Jaffe R. 1986, Reproductive Endocrinology: Physiology, Pathophysiology and Clinical Management, W.B. Saunders Company, Philadelphia, Pa., USA.):
1. The follicular phase during which several ovarian follicles are recruited, followed by the selection and the dominance of one follicle. This phase lasts approximately 12 days and is characterized by a progressive rise of serum estradiol levels and low progesterone levels. This phase is the result of the secretion of a hormone called FSH (“Follicle Stimulating Hormone”) by the anterior pituitary gland.2. A peri-ovulatory phase (also called ovulation) which lasts approximately 48 hours and is characterized by a sudden rise in serum LH (“Luteinizing Hormone”, another hormone secreted by the pituitary gland). This phase ends when the “corpus luteani” is formed. This phase includes the following sequence of events:
The Final Follicular Maturation:                The follicle steroidogenesis switches from a preferential secretion of estradiol to a preferential secretion of progesterone.        The oocyte resumes its meiosis.        
The Ovulation:                The follicle is ruptured and the oocyte leaves the ovary        
The Corpus Luteum Formation                The empty follicle is re-organized to form the corpus luteum.3. The luteal phase during which the corpus luteum secretes large amount of progesterone as well as somewhat smaller quantities of 17 OH-progesterone, estradiol, estrone and relaxin. This phase lasts approximately 14 days and depends of an appropriate secretion of LH by the pituitary gland. During the luteal phase, progesterone works together with estradiol on endometrial cells to provide an environment favorable for the embryo implantation.        
The luteal phase can be deficient. This can result from a deficit in progesterone secretion by the corpus luteum. In this case, serum progesterone levels are below 10 ng/ml. The luteal deficiency can also result from a shortening of the luteal phase (i.e. less than 11 days). The clinical consequences of a luteal phase deficiency are failure of embryo implantation, or a miscarriage if the pregnancy has already started (Yen S, and Jaffe R. 1986, Reproductive Endocrinology: Physiology, Pathophysiology and Clinical Management, W.B. Saunders Company, Philadelphia, Pa., USA.).
A luteal phase deficiency is a common characteristic of cycles during which follicular development is stimulated with pharmacological agents for the treatment of infertility. This has been reported both in anovulatory patients undergoing ovulation induction therapy, and in ovulatory patients undergoing stimulation of multiple follicular development prior to intra-uterine insemination (IUI) or prior to Assisted Reproductive Techniques (ART) such as in vitro fertilisation (IVF) and intra-cytoplasmic insemination (ICSI).
The luteal phase deficiency has been observed in cycles stimulated with clomiphene citrate, FSH/hMG, FSH/hMG with a GnRH agonist pre-treatment (“Gonadotrophin releasing hormone”) as well as FSH/hMG with a GnRH antagonist co-treatment (Beckers N G et al. 2003, Comparison of non-supplemented luteal phase characteristics following the administration of r-hCG, r-hLH or GnRH agonist to induce final oocyte maturation in in vitro fertilisation patients. J. Clin. Endocrinol. Metab. 88: 4186-4192; Pritts E. A. and Atwood A. K. 2002, Luteal support in infertility treatment: a meta-analysis of the randomized trials. Hum Reprod 17: 2287-2299). The luteal phase deficiency is mainly attributed to the elevated serum estradiol levels resulting from the pharmacological stimulation of the ovaries.
The pharmacological support of the luteal phase, also called “luteal supplementation”, is mandatory in infertility treatments in order to significantly increase the embryo implantation rate, the pregnancy rate and to reduce the miscarriage rate (Pritts E. A. and Atwood A. K. 2002, Luteal support in infertility treatment: a meta-analysis of the randomized trials. Hum Reprod 17: 2287-2299).
Two drugs are routinely used for the luteal support. The first is natural progesterone, the second is the human chorionic gonadotropin (hCG). Progesterone is administered intra-muscularly (IM) or vaginally. The therapeutic objective is to increase serum progesterone levels. HCG is administered intra-muscularly (IM) or sub-cutaneously (SC). HCG is a naturally occurring agonist of LH and therefore it stimulates progesterone secretion by the corpus luteum.
In ART treatments, a luteal support by hCG or progesterone IM significantly increases pregnancy rate (Pritts E. A. and Atwood A. K. 2002, Luteal support in infertility treatment: a meta-analysis of the randomized trials. Hum Reprod 17: 2287-2299). The odds to obtain a pregnancy with hCG compared to no luteal support is 2.72 (CI: 1.56-4.90; p<0.05) and with progestérone IM is 2.38 (CI: 1.36-4.27; p<0.05). Progesterone administered by vaginal route, although superior to no luteal support, is not as effective as progesterone IM. With vaginal progesterone the odds to obtain a pregnancy is 2.11 with a C.I. of 0.95-4.67 (NS). Furthermore, the relative efficacy of IM progesterone vs vaginal progesterone is 1.33 with a C.I. of 1.02-1.75, in favor of the IM route (p<0.05) (Pritts E. A. and Atwood A. K. 2002, Luteal support in infertility treatment: a meta-analysis of the randomized trials. Hum Reprod 17: 2287-2299).
The drawbacks of IM progesterone are: (i) the injections must be performed daily for more than two weeks, (ii) the progesterone solution is oily and therefore injections are painful, (iii) these injections can trigger an inflammatory reaction and even a sterile abcess, (iv) IM injections are not easy for self-administration by the patient therefore often requiring paramedical assistance.
The drawbacks of hCG as luteal support are: (i) its use is associated with a rare but potentially life-threatening adverse event called ovarian hyperstimulation syndrome (OHSS), (ii) it must be injected, (iii) it induces a false positive pregnancy test, delaying the pregnancy diagnostics, (iv) it is a biological product extracted from urine or from culture media containing animal sera, and therefore presents a, at least theoritical risk, of contamination by infectious particles (e.g. viruses or prions) (Reichl H et al., 2002 Prion transmission in blood and urines: what are the implications for recombinant and urinary-derived gonadotropins Hum Reprod 17: 2501-2508). For all these reasons many doctors refrain of using hCG as luteal support.